Galectin-3 interacts with PD-1 and counteracts the PD-1 pathway-driven regulation of T cell and osteoclast activity in Rheumatoid Arthritis.

Effects of Gal-3 on the PD-1 signaling axis are proposed to be inhibitory, meaning high Gal-3 levels in the complex synovial microenvironment are not desirable in RA. Preventing Gal-3's inhibitory role on PD-1 signaling could therefore be a therapeutic target in RA by affecting inflammatory T cell responses and osteoclasts.